To confirm the importance of phosphorylation of Asp-54 in vivo, we constructed the KD1113 mutant strain, which has D54N-MbrC instead of wild-type MbrC. Both KD1113 and the mbrC deletion mutant KD1108 were 50-fold more susceptible to bacitracin than UA159 (Table 3). Furthermore, real-time RT-PCR analysis revealed that transcription of mbrA in KD1113 was not induced by bacitracin, while the wild-type strain UA159 showed 50-fold mbrA induction in the presence of bacitracin (Table 3). These results support Metformin order the idea that Asp-54 is essential

for the activation of mbrA transcription by MbrC. Induction of SMU.302, SMU.862, and SMU.1856c by bacitracin was not seen in KD1108 or K1113, while induction of SMU.1479 against bacitracin remained (Table 3). Eight S. mutans genes (SMU.302, SMU.862, SMU.863, SMU.864, mbrA, mbrB, SMU.1479, SMU.1856c) were induced fourfold or more by bacitracin (Table 2). Ouyang et al. (2010) found that the promoter regions of SMU.302, SMU.862, and SMU.1856c have a consensus-specific inverted repeat sequence similar to that of mbrA. Tandem arrangements see more of SMU.862, 863, and 864 and mbrA and B suggest that induction of SMU.863 and 864 and mbrB against bacitracin is dependent on the upstream gene’s promoters. MbrC was associated with the transcriptional

regulation of these genes. In contrast, SMU.1479 has no consensus inverted repeat sequence and was not regulated by the MbrC protein, and Thalidomide so this gene may be regulated by another signaling system. Inactivation of these genes, with the exception of mbrAB, did not affect bacitracin resistance, confirming that induction of mbrAB transcription is important for S. mutans bacitracin resistance. MbrC and D belong to the family of ‘bacitracin-responsive’ TCS (Chong et al., 2008), of which B. subtilis bceRS has been described in detail (Rietkotter et al., 2008). Genes encoding such TCS are usually located adjacent to ABC

transporter genes. The levels of mbrAB, but not mbrCD, mRNA increased drastically in response to bacitracin. This seems to contradict our previous finding that the four mbr genes constitute a single operon (Tsuda et al., 2002). One explanation might be that the mbr gene cluster comprises two types of operon structure, namely the mbrABCD and mbrAB operons due to a terminator structure between mbrB and mbrC, and transcription of the latter may be selectively activated by bacitracin to a greater degree than that of the former. Indeed, we found a stemloop structure, followed by a thymine-rich sequence in the intergenic region between mbrB and C. The deduced amino acid sequence of mbrC resembles a TCS response regulator. Phosphorylation of the response regulator is ordinarily required for DNA binding to the promoter region of the target gene. MbrC binds to the promoter region of mbrA and its phosphorylation enhances this binding (Ouyang et al., 2010).

coli. In this work, we demonstrated that the mioC gene has functions related to biofilms, cell aggregation, motility, cell lysis and EPS production. As these physiologies may be important for P. aeruginosa virulence (Vasil & Ochsner, 1999; Shapiro et al., 2002; Rybtke et al., 2011), the mioC gene might be a useful therapeutic target for pathogenic bacteria. This work was supported by the MEST/NRF program (grant # 2009-0076488) to W.P. “
“Pseudomonas aeruginosa responds LDK378 concentration to phosphate limitation by inducing the expression of phosphate transport systems, phosphatases, hemolysins and a DNase, many of which are important for virulence. Here we report that under phosphate-limiting

conditions, P. aeruginosa produces a phosphate-free ornithine lipid (OL) as the primary membrane lipid. The olsBA (PA4350-PA4351) genes were highly induced under phosphate-limiting conditions. The production and structure of the OL was confirmed by MS, revealing diagnostic fragment ions and mainly C16 : 0 and C18 : 1 dialkyl chains.

It was shown that olsA is required Kinase Inhibitor Library molecular weight for production of these lipids and genetic complementation of the olsA∷lux mutant restored OL production. Studies in other bacteria have correlated increased resistance to antimicrobial peptides with the production of OLs. Here it was demonstrated that resistance to antimicrobial peptides increased under phosphate-limiting conditions, but OLs were not required for this increased resistance. OL production was also not required for virulence in the Caenorhabditis elegans infection model. The production of OLs is

a strategy to reduce phosphate utilization in the membrane, but mutants unable to produce OLs have no observable phenotype with respect to growth, antibiotic resistance or virulence. The response to phosphate limitation in Pseudomonas aeruginosa is diverse and includes the expression of phosphate acquisition systems, hemolysins, catalase, an alternative type II secretion system phosphatases, phenazines, pyoverdine, PQS and several auxiliary regulatory Florfenicol systems (Ostroff et al., 1989; Hassett et al., 1992; Ball et al., 2002; Lewenza et al., 2005; Jensen et al., 2006; Zaborin et al., 2009). We identified an extracellular DNase that is expressed and secreted under phosphate-limiting conditions and is required for utilizing extracellular DNA as a nutrient source of phosphate (Mulcahy et al., 2010). There is accumulating evidence that phosphate limitation is an environmental challenge faced during an infection and therefore many of the phosphate-regulated virulence factors are likely important in vivo (Frisk et al., 2004). Phosphate limitation occurs as a result of surgical injury to the gastrointestinal tract and leads to the induction of phosphate-regulated virulence factors in P. aeruginosa (Long et al., 2008). Another adaptation to phosphate-limiting conditions is the production of membrane lipids with non-phosphate-containing head groups.

, 1991; Barber et al., 1997; Slater et al., 2000; Dow et al., 2003; Fouhy et al., 2006; Ryan et al., 2006). RavS/RavR affect cell motility, exopolysaccharide synthesis, extracellular enzyme secretion and biofilm production

HM781-36B in vitro by regulating the expression of the corresponding genes by cyclic-di-GMP synthesis or hydrolysis and activation of RavR (He et al., 2009 and our unpublished data). XCC3107 was identified by genome-scale mutagenesis and was found to be involved in protease production and virulence (Qian et al., 2008). HrpG is an important regulator that controls the expression of the type III secretion system by interacting with the downstream AraC-family transcription factor, HrpX (Noel et al., 2001). However, HrpG is an orphan RR whose cognate histidine kinase has not been identified to date. In this study, we have identified an orphan RR (VemR)

that is required for virulence and adaptation of Xcc. The vemR gene resides in an operon that consists of the rpoN2, vemR and fleQ genes (Fig. 1a). The ATM/ATR inhibitor clinical trial rpoN2 gene encodes a sigma 54 factor that is involved in nitrogen assimilation, nitrogen fixation, utilization of carbon sources, motility, alginate biosynthesis and virulence (Reitzer & Schneider, 2001; Yang et al., 2009). The fleQ gene encodes a sigma 54 factor cognate activator that is essential for normal flagellation and transcription of the promoters of the fliE, fliL, fliQ, flgB, flgG, flhF and flhBA genes in Xcc strain XC17 (Hu et al., 2005; Yang et al., 2009). It was observed that insertional inactivation of the fleQ gene resulted in impaired motility and virulence in Xcc strain XC17 (Yang et al., 2009). However, insertional inactivation of the vemR gene, which probably affects the expression of the fleQ gene, has no significant effect on virulence in Xcc ATCC 33913 (Qian et al., 2008). To avoid

unwanted polar effects, ΔvemR and ΔfleQ mutants were generated by in-frame deletion of the vemR and fleQ genes, respectively. Phenotyping demonstrated that mutation of the vemR gene severely affected Xcc virulence, exopolysaccharide production and motility (Fig. 1b, c and 2), whereas mutation of the fleQ gene showed less phenotypic effects in Xcc strain 8004 Sclareol (Fig. 4). Similar phenotypes were observed on deletion of the vemR gene in Xcc ATCC 33913 (data not shown). Moreover, the double-deletion mutant ΔvemR/ΔfleQ had a phenotype similar to the single mutant ΔfleQ (Fig. 4 and data not shown), suggesting that insertion inactivation of the vemR gene in Xcc ATCC 33913 might inactivate both vemR and fleQ genes simultaneously. Previous studies have shown that FleQ is an important regulator of the expression of flagella and exopolysaccharide biosynthesis genes in Pseudomonas aeruginosa (Dasgupta et al.

Therefore, the clone libraries represent (i) inshore at Daydream Island during summer, (ii) inshore at Daydream Island during winter, signaling pathway (iii) offshore at Deloraine Island during summer and (iv) offshore at Deloraine Island during winter. Triplicate PCR reactions were performed for each of the four replicate biofilm samples from each of these representative two sampling locations (total of eight) and two sampling times (overall total 16), and were pooled accordingly

for construction of the four clone libraries. Samples were then purified using the MinELUTE PCR Clean-Up Kit (Qiagen) and cloned using a TOPO-TA Cloning Kit (Invitrogen) according to the manufacturer’s instructions. Afterwards, blue-white screening colonies were checked for correct insert size using a colony PCR method using primers 63F/1389R. Per clone library, 96 randomly picked clones were then dispersed in LB media and 10% glycerol in 96-well plate format and sent to the Australian Genome Research Facility Ltd. (Brisbane, Australia) for purification and sequencing using an ABI3730 XL Automatic

DNA Sequencer. Retrieved sequences were trimmed and analysed manually using buy PF-6463922 Chromas Lite 2.33 (Technelysium Pty Ltd., Australia), and submitted to the Greengenes NAST Aligner (DeSantis et al., 2006) for alignment of sequences to the Greengenes database. Greengenes NAST-aligned 16S rRNA gene sequences were checked for chimeras using bellerophon Version 3 (Huber et al. 2004), and identified chimeras were excluded from further analysis. The NAST-aligned 16S rRNA gene sequences were submitted to the Greengenes batch sequence classifier [http://greengenes.lbl.gov/cgi-bin/nph-classify.cgi], and taxonomic assignments for each sequence were recorded using NCBI taxonomy. All sequences were submitted to

the GenBank Database (Accession numbers: JF261700–JF262029). Bacterial 16S rRNA genes were PCR amplified using the same reaction mixture and conditions as outlined for clone libraries, except that fluorescently labelled 5′Cy5-labelled 63F (Sigma-Aldrich) Palbociclib was used (adapted from Wilson et al., 2008). Each individual biofilm sample was amplified in three replicate PCR reactions. The amplicons were pooled, purified and quantified as above. Each purified product (150 ng) was digested with the restriction enzyme MspI (New England Biolabs) according to the manufacturer’s instructions. Digested fragments were desalted using the DyeEx 2.0 Spin Kit (Qiagen) and vacuum dried for 40 min at low temperature in the dark. Terminal restriction fragments (T-RFs) were resolved and visualized using the CEQ 8800 Genetic Analysis System (Beckman-Coulter, Fullerton, CA) with a 600 bp size standard (Beckman-Coulter). Replicate samples were compared using the software T-align (Smith et al., 2005) with a range of 0.5 bp peak area to determine the consensus peaks between duplicates.

Therefore, the clone libraries represent (i) inshore at Daydream Island during summer, (ii) inshore at Daydream Island during winter, high throughput screening compounds (iii) offshore at Deloraine Island during summer and (iv) offshore at Deloraine Island during winter. Triplicate PCR reactions were performed for each of the four replicate biofilm samples from each of these representative two sampling locations (total of eight) and two sampling times (overall total 16), and were pooled accordingly

for construction of the four clone libraries. Samples were then purified using the MinELUTE PCR Clean-Up Kit (Qiagen) and cloned using a TOPO-TA Cloning Kit (Invitrogen) according to the manufacturer’s instructions. Afterwards, blue-white screening colonies were checked for correct insert size using a colony PCR method using primers 63F/1389R. Per clone library, 96 randomly picked clones were then dispersed in LB media and 10% glycerol in 96-well plate format and sent to the Australian Genome Research Facility Ltd. (Brisbane, Australia) for purification and sequencing using an ABI3730 XL Automatic

DNA Sequencer. Retrieved sequences were trimmed and analysed manually using Poziotinib datasheet Chromas Lite 2.33 (Technelysium Pty Ltd., Australia), and submitted to the Greengenes NAST Aligner (DeSantis et al., 2006) for alignment of sequences to the Greengenes database. Greengenes NAST-aligned 16S rRNA gene sequences were checked for chimeras using bellerophon Version 3 (Huber et al. 2004), and identified chimeras were excluded from further analysis. The NAST-aligned 16S rRNA gene sequences were submitted to the Greengenes batch sequence classifier [http://greengenes.lbl.gov/cgi-bin/nph-classify.cgi], and taxonomic assignments for each sequence were recorded using NCBI taxonomy. All sequences were submitted to

the GenBank Database (Accession numbers: JF261700–JF262029). Bacterial 16S rRNA genes were PCR amplified using the same reaction mixture and conditions as outlined for clone libraries, except that fluorescently labelled 5′Cy5-labelled 63F (Sigma-Aldrich) Clomifene was used (adapted from Wilson et al., 2008). Each individual biofilm sample was amplified in three replicate PCR reactions. The amplicons were pooled, purified and quantified as above. Each purified product (150 ng) was digested with the restriction enzyme MspI (New England Biolabs) according to the manufacturer’s instructions. Digested fragments were desalted using the DyeEx 2.0 Spin Kit (Qiagen) and vacuum dried for 40 min at low temperature in the dark. Terminal restriction fragments (T-RFs) were resolved and visualized using the CEQ 8800 Genetic Analysis System (Beckman-Coulter, Fullerton, CA) with a 600 bp size standard (Beckman-Coulter). Replicate samples were compared using the software T-align (Smith et al., 2005) with a range of 0.5 bp peak area to determine the consensus peaks between duplicates.

This article supports the standardization of VFR traveler definitions based on objective criteria and provides illustrations of the application of this definition through an illustrated approach to risk assessment based on these criteria and the differentials in the determinants of health between Talazoparib datasheet source and destination regions. Methods. A working group was established by the Migration Health Sub-committee, International Society for Travel Medicine to assess the literature on VFR travel and health, review an evidence-based approach to managing health risk related to travel, and to propose criteria-based definition for VFR travel. The new

definition of a VFR is a traveler whose primary purpose of travel is to visit friends or relatives where there is a gradient of epidemiological risk between home and destination. Results. A case scenario discussion of VFR travel defined by criteria and risk assessment based on differential determinants of health is presented in this article. Discussion. The goal of this article is to encourage discussion on travel health evaluation for the most “at risk” populations and to standardize the application of clinical, public health, and research approaches to defining VFR travelers in a risk management context. The group of travelers commonly referred to as visiting

friends or relatives (VFR) travelers has been identified as being at increased risk of a number of travel-associated diseases.1–5 INCB024360 mw The morbidity and mortality they experience appears to be more frequent and clinically significant than

in other groups such as tourists, students, business, and expatriate travelers. Recent changes in patterns of global travel, increasing numbers of international travelers, and changes in the dynamics of global networking are leading to the re-evaluation of the approach to “VFR traveler” and risk assessment for health management and disease prevention purposes. A definition updating the approach to the VFR traveler has recently been published.6 The purpose of applying a new definition of VFR travel Mephenoxalone is to facilitate three outcomes: reducing the morbidity and mortality gap1 believed to exist for VFR travelers, improving travel health research through the use of comparable population definitions, and to inform and influence public health policy and program design. The goal of this paper is to illustrate the use of the proposed VFR definition and framework by providing mock travel case scenarios demonstrating the application of the definition in selected risk events. These scenarios will both illustrate the complexity and rigor required in risk assessment for VFR travelers and provide examples for health professionals in the application of risk assessment leading to counseling and interventions to promote and protect the health of VFR travelers. An objective approach to the definition of a VFR traveler is as follows.

Genetic modifications, such as the targeted inactivation of genes or artificial controlled (over)expression, require the use of selectable markers for efficient isolation and selection of transformed cells. So far, only a few selectable markers for transformation of H. jecorina have been reported, including pyr4, amdS, hph and ptrA gene (Penttiläet al., 1987; Gruber et al., 1990; Mach et al., 1994; Kubodera et al., 2002). Auxotrophic markers that complement specific nutritional requirements have the advantage over dominant markers in high transformation efficiencies (Gruber et al., 1990) and because

selection for dominant marker genes requires the addition of toxic compounds to the growth media. Besides their toxicity, which may affect cellular functions, the cost of many PD0332991 research buy of these compounds precludes their use in large-scale processes. Some of the most commonly applied marker genes are wild-type PF-562271 manufacturer alleles of genes that encode key enzymes involved in different metabolic pathways including nucleotide or amino acid biosynthesis (Lin Cereghino et al., 2001). The most prominent example for an auxotrophic marker in filamentous

fungi is probably the pyr4 gene, which encodes orotidine-5′-phosphate decarboxylase, an essential enzyme in pyrimidine biosynthesis. The ease with which auxotrophic strains can be manipulated and the low cost of the supplementing chemicals have contributed to the construction of laboratory strains with various combinations of auxotrophic markers. Today, the low availability of markers limits multiple genetic manipulations toward metabolic Orotic acid engineering of H. jecorina. Collectively, the development of new auxotrophic markers for H. jecorina is significant and timely. In this study, a novel transformation system for H. jecorina was characterized based on a strain deficient in hxk1 (encoding hexokinase) as the recipient strain, the hxk1 gene as an

auxotrophic marker and d-mannitol as both a high-pressure selective agent and osmotic stabilizer. Here, we present a high efficient and reproducible transformation system based on a carbon source-dependent selection strategy for filamentous fungi. Hypocrea jecorina uridine auxotrophic pyr4-negative strain TU-6 (ATCC MYA-256) and its hxk1 deletion strain TU-6H were maintained on minimal medium (MM) supplemented with 10 mM uridine when necessary (Hartl & Seiboth 2005). Hypocrea jecorina strain TU-6H was used as the transformation host. Plasmids were propagated in Escherichia coli strain DH5α (Invitrogen). Plasmid pIG1783 (Pöggeler et al., 2003), carrying the enhanced green fluorescent protein (EGFP) expression cassette, was kindly donated by Professor Ulrich Kück. To measure growth on different carbon sources, H. jecorina strains were grown on potato dextrose agar plates.

HbA1c was 12.4%; fasting total cholesterol 5.92mmol/L (NR 2.5–5). The patient was prescribed oestrogen replacement and no adjustments were made to diet or insulin. Over several months, mood and energy improved and weight fell from 110kg to 81kg, HbA1c dropped to 7.6%, cholesterol was 2.56mmol/L and insulin dosage halved. The impact of menopausal symptoms on health and wellbeing

is often underestimated. In selected post-menopausal women with type 2 diabetes, short-term selleck treatment with hormone replacement therapy may be useful if benefits obtained outweigh potential risks. Copyright © 2010 John Wiley & Sons. “
“Diabetes in pregnancy, including Type 1 diabetes, Type 2 diabetes, and gestational diabetes, is increasingly common and now complicates over 20% of pregnancies in some populations. While interpretation of epidemiologic data is difficult due to variation in screening practices and diagnostic criteria, it has become clear that the prevalence of both obesity, as the key risk factor, and diabetes in pregnancy have increased. The impact of diabetes in pregnancy on the baby may be Alectinib research buy ameliorated by clinical intervention before and during pregnancy and has been shown to be

cost-effective. The long-term benefits of clinical intervention for diabetes in pregnancy on a population basis have yet to be proven, but if the intervention includes prepregnancy care and postnatal management of both mother and baby (including support for physical activity and healthy eating), these are likely to be of major public health importance. “
“There Hydroxychloroquine nmr is a lack of consensus among expert bodies regarding the virtue of screening for gestational diabetes mellitus (GDM). Central to the debate is the significance of GDM as a disease entity. A variety of screening tests are endorsed by different professional organizations. Not all organizations recommend screening to decide which patients are offered definitive testing for GDM. Furthermore,

international consensus regarding glycemic thresholds to define GDM has not as yet been achieved. In the US, Canada, and Australasia the 50-g, 1-hour glucose test is the recommended screening test. Prevalence rates of GDM vary with the choice of glucose thresholds for both screening and definitive tests. Glucose challenge test results are poorly reproducible and depend on timing of the last meal. Simple, and preferably single, screening and/or diagnostic tests are the ideal. Any screening test will have to be evaluated in relation to the new HAPO diagnostic criteria for GDM. “
“The aim of this survey was to establish the limitations of open loop continuous subcutaneous insulin infusion (CSII) as perceived by current users of the technology, and to ascertain their interest in and requirements for a non-electronic implantable closed loop insulin pump, INSmart, currently under development for the treatment of type 1 diabetes.

coelicolor (Yang et al., 2006). The specificity for dCMP incorporation into pORF102 leaves the possibility that either the

Palbociclib first or the second nucleotide of the 3′-end of pAL1 (… GCAGG-3′) may serve as a template for the deoxynucleotidylation reaction. In this study, we identified the gene product of pAL1.102 as a protein that is associated with both termini of the linear Arthrobacter plasmid pAL1. The proposed TP – at least when fused to MBP to ensure solubility – was not capable of specifically recognizing telomeric pAL1 DNA in vitro. However, in an in vitro deoxynucleotidylation assay, the pORF102 protein specifically incorporated dCMP, complementary to the 3′-ends of pAL1. This is consistent with its presumed role as a protein primer in DNA replication. The financial support of the Deutsche Forschungsgemeinschaft is gratefully acknowledged (FE 383/11). We thank Prof. Dr R. Brandsch (University of Freiburg, Germany) for kindly providing the vector pART2, and Prof. Dr A. Steinbüchel (Münster) for access to the phosphoimager. We also thank Manuel Tomm for initial EMSA experiments, and Gabriele Niester and Almut Kappius for technical assistance. Table S1. Primers and ssDNA template

Daporinad nmr used in this study. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Many bacteria produce siderophores for sequestration of growth-essential iron. Analysis of the Salinispora genomes suggests that these

marine actinomycetes support multiple hydroxamate- and phenolate-type siderophore pathways. We isolated and characterized desferrioxamines (DFOs) B and E from all three recognized Salinispora species and linked their biosyntheses in S. tropica CNB-440 and S. arenicola CNS-205 to the des locus through PCR-directed mutagenesis. Gene inactivation of the predicted iron-chelator Selleckchem CHIR 99021 biosynthetic loci sid2-4 did not abolish siderophore chemistry. Additionally, these pathways could not restore the native growth characteristics of the des mutants in iron-limited media, although differential iron-dependent regulation was observed for the yersiniabactin-like sid2 pathway. Consequently, this study indicates that DFOs are the primary siderophores in laboratory cultures of Salinispora. Siderophores are small molecules secreted by bacteria to sequester growth-essential ferric iron that is poorly soluble under neutral pH and aerobic conditions (Neilands, 1995). The structures of siderophores vary considerably and are often suited to the environmental niche of the producing bacterium. For example, amphiphilic siderophores possess hydrophobic fatty acid chains that enable them to remain associated with the cell membrane (Martinez et al., 2003) – an attribute particularly advantageous in pelagic marine environments where dilution occurs rapidly.

S3). Increased sensitivity to ETBR was also observed in complemented dcm strains (Table 3). PI3K Inhibitor Library in vivo These data indicate that there is an inverse relationship between the presence of the dcm gene and ETBR resistance. Based on the qPCR and drug susceptibility

data, our model is that increased sugE expression in the absence of Dcm is responsible for ETBR resistance. The results of Sulavik et al. and Nishino et al. indicate that there are several transporter genes that are linked to ETBR resistance via overexpression and knockout studies including acrAB, acrEF, emrE, mdfA, tolC, yhiUV, and ydhE (Nishino & Yamaguchi, 2001; Sulavik et al., 2001). The biggest effect was with acrAB, as the MIC increased > 32-fold when acrAB was overexpressed and decreased > 250-fold when acrAB was disrupted. Thus, we were interested to know if there are other transporters in addition to SugE that are up-regulated in the absence of cytosine DNA

methylation that could contribute to ETBR resistance. We are currently using DNA microarrays to generate gene expression profiles of wild-type cells, dcm knockout cells, and wild-type cells treated with 5-azacytidine SRT1720 research buy at both logarithmic phase and stationary phase. In initial experiments, we observed no transporters from the list above that were up-regulated both in the absence of dcm and presence of 5-azacytidine (> twofold) (K.T. Militello, R.D. Simon, A.H. Mandarano, S.M. Hennick & A.C. DiNatale, in preparation). Moreover, none of the transporters listed above were up-regulated > twofold in the absence of dcm alone. Thus, our model is that SugE is responsible for the ETBR resistance observed, but it is not possible at this point to rule out the effect of other transporters

on ETBR resistance or small contributions by multiple transporters that result in a detectible change in ETBR resistance. In total, our experiments have uncovered a new and unexpected phenotype for the loss of Dcm; changes in sensitivity to ETBR. Our data also brings up the possibility that potential changes in DNA methylation levels due to nutritional status, presence of restriction-modification systems, and/or epigenetic mechanisms may influence the sensitivity of prokaryotes to antibacterial from compounds through changes in gene expression and thus link specific environments to differential antibiotic resistance. We thank the Geneseo Foundation for funding, Ashok Bhagwat (Wayne State University) for plasmid DNAs, and Devin Chandler-Militello, Sarah Ackerman, Leanne Chen, and Erika Valentine for manuscript editing. “
“The presence of toxigenic cyanobacteria capable of biosynthesis of cylindrospermopsin (CYN) was measured in 24 water samples collected from the lakes Bytyńskie (BY) and Bnińskie (BN) in the Western Poland. The study also covered analysis of toxigenicity and production of CYN by the culture of Cylindrospermopsis raciborskii isolated from BY.